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(2019). https://pubmed.ncbi.nlm.nih.gov/31527311/ DOI: 10.1172/jci129710","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Hepatocytes and small-intestinal enterocytes","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"48be3158-f1ba-58d2-8b93-dfcf52aab054","evidence_kind":"source_excerpt","locator":"Lines 279-290","start_line":279,"end_line":290,"excerpt":"### mn-trans-slc30a10-double-versus-global\nCombined liver and small-intestine Slc30a10 deficiency caused manganese excess that was less severe than in whole-body deficient mice.\nCondition category: machinery_impairment\nnutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: Deleting the liver and gut exporter did not reproduce the full severity of deleting it everywhere.\norganism: Mus musculus\ntissue_or_cell_type: Hepatocytes and small-intestinal enterocytes\nexperimental_model: Whole-body and tissue-specific Slc30a10 knockout mice\nlimitations: The residual difference suggests other sites or adaptation; it does not identify a specific untested tissue.\nexposure: Liver-and-small-intestine Slc30a10 deficiency compared with controls and whole-body deficiency.\ncross_nutrient: false\n[mn-trans-31527311] Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. 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